Cigarette smoking is associated with increases in plasma
triglycerides and decreases in plasma
high density-lipoprotein-cholesterol concentration. These changes not only increase risk of
coronary heart disease but also are secondary to resistance to
insulin-stimulated
glucose uptake or hyperinsulinaemia. To see whether there is a relation between cigarette smoking and
insulin-mediated
glucose uptake we measured plasma
lipid and
lipoprotein concentrations, plasma
glucose and
insulin response to an oral
glucose challenge, and
insulin-mediated
glucose uptake in 40 matched healthy volunteers (20 non-smokers, 20 smokers). Smokers had significantly higher mean (SEM)
very-low-density-lipoprotein triglycerides (0.66 [0.10] vs 0.39 [0.03] mmol/l, p less than 0.02) and
cholesterol (0.45 [0.06] vs 0.23 [0.04] mmol/l, p less than 0.005) concentrations and lower
high-density-lipoprotein cholesterol concentrations (1.16 [0.05] vs 1.51 [0.08] mmol/l, p less than 0.001). Although plasma
glucose concentrations in response to the oral
glucose load were similar in the two groups, plasma
insulin response of the smokers was significantly higher (p less than 0.001). Finally, smokers had higher steady-state plasma
glucose concentrations in response to a continuous infusion of
glucose,
insulin, and
somatostatin (8.4 [0.2] vs 5.0 [0.3] mmol/l, p less than 0.001), despite similar steady-state plasma
insulin concentrations. The findings show that chronic cigarette smokers are
insulin resistant, hyperinsulinaemic, and dyslipidaemic compared with a matched group of non-smokers, and may help to explain why smoking increases risk of
coronary heart disease.